Is There a Developmental Component to the Risk for Depression?

Is There a Developmental Component to the Risk for Depression?

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Philadelphia, PA, December 10, 2007 – Psychiatrists remain divided as to how to define and classify the mood and anxiety disorders, the most common mental disorders. Committees across the globe are currently pondering how best to carve nature at its anxious joints for the fifth version of the Diagnostic and Statistical Manual (DSM-V), the “gold standard” reference book for psychiatrists. Only recently has the process of refining the diagnostic system been informed by high quality longitudinal data. An important new study of this type was published in the December 1st issue of Biological Psychiatry.

Ian Colman, Ph.D., the lead author, notes, ““Rarely have classification systems in psychiatry considered the nature of symptoms of depression and anxiety over time; however research into trajectories of alcohol abuse and antisocial behaviour shows that accounting for symptoms over time may help in better understanding causes and outcomes of these disorders.” Colman and colleagues at the University of Cambridge in England and the Medical Research Council National Survey of Health and Development (now called the MRC Unit for Lifelong Health and Ageing), using fundamental ideas about the life-course origins of common mental illnesses, statistical techniques for handling large quantities of longitudinal information and one of the longest running cohort studies in the world, were able to analyze data by grouping people according to their symptoms of anxiety and depression over a 40-year period.

The researchers were able to identify six courses of mental health, ranging from those with repeated severe symptoms to those in good mental health, while others fluctuated in between. Dr. Colman adds, “The usefulness of characterizing people by their experience over time became evident when we investigated markers of early development, and found that those with poorer mental health over time were more likely to be smaller at birth and tended to reach developmental milestones later than those with good mental health.”

John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments, “The study by Colman and colleagues suggests that children with low weight during infancy or slight developmental delays may be at greater risk for developing depression. How does this risk work? After all, it is extremely unlikely that adults bear emotional scars from very subtle delays in their standing or walking.” The authors explain that their findings support a proposed “fetal programming” model for depression and anxiety, which posits that prenatal stress may result in permanent maladaptive changes to the developing fetal brain. Particularly notable was the fact that differences with regards to early development were apparent not only for those with severe problems with mental health, but also for those with mild to moderate symptoms of depression and anxiety over time. Dr. Krystal adds that it may also be “that genes that are involved in shaping the development of the brain and the emergence of particular behaviors during infancy also influence the development of brain circuits that influence the risk for depression later in life.”

The authors hope that this rich-data/whole life approach may foster insights into the causes of brief versus persistent and early vs late onset disease processes, and eventually identify underlying mechanisms responsible for such different life course outcomes in mental ill-health.

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Notes to Editors: The article is “A Longitudinal Typology of Symptoms of Depression and Anxiety Over the Life Course” by Ian Colman, George B. Ploubidis, Michael E.J. Wadsworth, Peter B. Jones and Tim J. Croudace. Drs. Colman, Ploubidis, Jones, and Croudace are affiliated with the Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom. Dr. Wadsworth is with the Medical Research Council National Survey of Health and Development, Department of Epidemiology and Public Health, University College London Medical School in London, United Kingdom. The article appears in Biological Psychiatry, Volume 62, Issue 11 (December 1, 2007), published by Elsevier.

Full text of the article mentioned above is available upon request. Contact Jayne M. Dawkins at (215) 239-3674 or ja.dawkins@elsevier.com to obtain a copy or to schedule an interview.

About Biological Psychiatry This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Commentaries, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly.

Biological Psychiatry is ranked 4th out of the 95 Psychiatry titles and 16th out of 199 Neurosciences titles on the 2006 ISI Journal Citations Reports® published by Thomson Scientific.

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